Calorie-dense Diet Research Articles

Hypoglyceamic and Hepatoprotective Potentials of Dichloromethane (DCM) Fraction of Gongronema Latifolium Extract in Streptozotocin-Induced Diabetic Wistar Rats

Diabetes is a chronic health issue with devastating but preventable consequences. The increasing proportion of the aging population, intake of calorie-dense diets, weight problems and sedentary lifestyles have been directly implicated in the increased number of diabetics globally. Furthermore, diabetes confers a huge economic burden due to its management costs, especially in low income countries. This study investigated the hypoglyceamic and hepatoprotective potentials of the dichloromethane (DCM) fraction of G. latifolium stem bark extract on some biochemical parameters in streptozotocin-induced hyperglycemic rats. A total of thirty (30) Wistar rats were randomly assigned into five (5) groups with six (06) animals per group. Type 2 diabetes was induced with intraperitoneal administration of streptozotocin in Groups 2 – 4, with animals in Groups 1 and 2 acting as normal and untreated diabetic controls, respectively. Group 3 rats were treated with the standard drug, metformin, while groups 4 and 5 were orally administered 200 and 400 mg/kg body weight of DCM fraction of G. latifolium stem bark extract. Changes in the body weight, biochemical assays (ALT, AST, total protein, albumin and urea), and expression levels of selected genetic markers, as well as the changes in liver histology, were determined and compared. Data obtained from this study show that the fasting blood glucose levels in hyperglycemic rats were significantly (p < 0.05) reduced, and the body weight steadily increased in rats treated with both doses of the DCM fraction of G. latifolium stem bark extract compared to the untreated diabetic rats. Total protein, AST and ALT levels, but not albumin levels, were significantly (p < 0.05) increased in rats treated with both doses of the extract. In addition, administration of the extracts significantly (p < 0.05) reversed the streptozotocin-induced repression of NRF2 and CAT expression in diabetic rats. Furthermore, histology results show an improvement in the liver architecture in the rats treated with the extract. The results from this study show that the DCM fraction of g. Latifolium stem bark extract possesses hypoglycemic, hepatoprotective and anti-diabetic activities and could be used in the management of diabetes.

Characterizing MetALD in a Nonhuman Primate Model using High Fat and Sucrose Diet and Chronic Binge Alcohol Administration

Mechanisms leading to metabolic and alcohol associated liver disease (MetALD) are not clearly delineated. This study examined the differential regulation of markers of hepatic mitochondrial function in nonhuman primates fed a high fat/high sucrose (HFSD) and administered chronic binge alcohol (CBA) or vehicle as compared to control-fed animals. We hypothesized that markers of hepatic dysregulation due to HFSD will be further altered by the combination of CBA/HFSD. Eight rhesus macaques were fed HFSD (27% sucrose and 42% fat, by kcal) with n=4 receiving vehicle and n=4 receiving 13-14g/kg/wk of ethanol through a gastric catheter. Rhesus macaques fed standard primate chow were used as reference controls (n=4-6). Liver RNA was isolated for determining expression of genes regulating mitochondrial biogenesis and function using RT-qPCR. Results were analyzed using one-way ANOVA and post-hoc pairwise multiple comparisons were performed using Tukey’s method, with alpha set to 0.05. Expression of inflammatory genes was significantly altered across the groups (p<0.05). HFSD increased tumor necrosis factor alpha (p=0.01), interleukin 1-beta (p=0.04), cluster of differentiation 38 (p=0.01), and transforming growth factor beta (p=0.01) expression compared to control. Both HFSD and CBA/HFSD increased interleukin-10 compared to control (p=0.02, p=0.03). Gene expression of mitochondrial function and oxidative stress regulators were significantly altered across the groups (p<0.05). CBA/HFSD decreased expression of peroxisome proliferator-activated receptor-gamma coactivator-1 beta (p=0.04) and nuclear respiratory factor 2 (p=0.04) compared to control. Both HFSD and CBA/HFSD decreased peroxisome proliferator-activated receptor alpha expression compared to control (p=0.01, 0.01). HFSD decreased superoxide dismutase 2 (SOD2) expression compared to control (p=0.01) and increased uncoupling protein 2 (p=0.01). SOD2 expression was increased only in CBA/HFSD compared to HFSD (p=0.01). These results reveal marked HFSD-mediated increases in markers of inflammation and CBA/HFSD-mediated changes in markers of mitochondrial function regulation and oxidative stress regulation. These findings suggest a greater impact of calorie-dense diets than CBA on hepatic inflammation and a combined impact of CBA and HFSD on mitochondrial regulation. Ongoing studies will examine oxidative phosphorylation complex protein activities and expression to elucidate and integrate HFSD or CBA mediated changes in hepatic bioenergetic capacity. Supported by F30AA030910, P60AA009803, and T32AA007577. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Obesity-Resistant Mice on a High-Fat Diet Display a Distinct Phenotype Linked to Enhanced Lipid Metabolism.

Individually, metabolic variations can significantly influence predisposition to obesity in the form of the obesity-prone (super-responders) and obesity-resistant (non-responders) phenotypes in response to modern calorie-dense diets. In this study, C57BL/6J mice (n = 76) were randomly assigned to either a low-fat diet (LFD) or a high-fat diet (HFD) for 6 weeks, followed by selection of the normally obese (HFD), non-responders (NR), super-responders (SR), or super-responders switched back to the low-fat diet (SR-LFD) for an additional 8 weeks. SR mice showed the highest gains in body weight, lean and fat body mass, and total and free water, in part due to increased feed efficiency, despite having a respiratory exchange ratio (RER) similar to that of NR mice. A switch to the LFD was sufficient to revert most of the observed physiological changes in the SR-LFD mice; however, voluntary physical activity and exercise capacity did not return to the basal level. NR mice showed the highest food intake, lowest feed efficiency, increased oxygen consumption during the light (rest) cycle, increased physical activity during the dark (active) cycle, and increased heat production during both cycles. These variations were observed in the absence of changes in food intake and fecal parameters; however, NR fecal lipid content was lower, and the NR fecal microbiome profile was characterized by reduced abundance of Actinobacteria. Taken together, our findings suggest that NR mice showed an increased ability to metabolize excessive dietary fats in skeletal muscle at the expense of reduced exercise capacity that persisted for the duration of the study. These findings underscore the need for further comprehensive investigations into the mechanisms of obesity resistance, as they hold potential implications for weight-loss strategies in human subjects.

Imagined foodways and rejected biopedagogies: Rural children's perspectives of rural foodways

AbstractRural residency is an independent risk factor for being overweight, but little is known about why this is so. The purpose of our study was to gain insight into what Norwegian rural children say about a rural diet in comparison to an urban one. Child‐friendly methods were used. We found a discrepancy between what the children said they eat – traditional, ‘healthy’ foods, and what they ate – largely ultra‐processed foods. We explored this by using the frameworks of imagined foodways and biopedagogies. Their imagined foodways were rooted in notions of ‘traditional food’, connected to surrounding nature and a history of farming and hunting. Urban people were perceived as eating an inferior diet of very unhealthy and ultra‐processed foods of which they do not know the origin of. As a result, the children rejected specific health‐ and nutrition recommendations that were incompatible with their notions of traditional foods, leading to a more calorie dense diet than their urban counterparts. Our research adds to knowledge on what role a rural diet can play on the prevalence of overweight in rural areas, and how biopedagogies can be recontextualized within different cultural fields.

Metabolic Syndrome and Its Associated Factors among Type 2 Diabetic Patients in Southwest Ethiopia, 2021/2022.

Background Metabolic syndrome is one of the leading global public health and clinical challenges, with increasing prevalence figures ranging from 10% to as high as 84%. There is a 5-fold increase in metabolic syndrome associated with type 2 diabetes and a 2-fold increase associated with the development of cardiovascular disease. The calorie-dense diet and sedentary life patterns are the most important contributory factors that have been established. Objective This study is aimed at assessing metabolic syndrome and its associated factors among patients with type 2 diabetes attending chronic follow-up units at hospitals in Southwest Ethiopia, in 2020. Methods This study was conducted at hospitals in Southwest Ethiopia, using an institutional-based cross-sectional study design from September 1, 2020, to August 30, 2021. Data was collected from 422 type 2 diabetics through face-to-face interviews using structured and pretested questionnaires. Data were entered into Epi-data version 4.4.1 and exported for analysis to the Statistical Package for Social Sciences 25. The magnitude of metabolic syndrome was determined by using the National Cholesterol Education Program Third Adult Treatment Panel III criteria. Bivariate and multivariable logistic regression analyses were used to evaluate associated factors for the outcome variable. A P value of less than 0.05 was considered statistically significant. Result and Conclusion. Out of the 422 sample sizes, 394 type 2 diabetics participated in this study, giving a response rate of 93.36%. The overall prevalence of metabolic syndrome among type 2 diabetics in this study was 68.3%, using the National Cholesterol Education Program and Third Adult Treatment Panel criteria. The associated factors for metabolic syndrome among type 2 diabetics are urban residency, old age, physical inactivity, salt intake, inadequate fruit and vegetable consumption, palm oil, and eating meat.

Trends in The Intake oF Food Groups Among Different Age Groups

Although there has been a vast increase in nutritional knowledge, a healthy dietary pattern is still established due to a lack of knowledge, availability, and accessibility. Even if vegetables are consumed higher percentage of starchy vegetables is consumed hence a balanced and adequate diet is still not followed. This research collected data from different cities of Pakistan via a questionnaire which was filled both face to face as well as online. The sample size was 60 with 10 people from each group. Data was collected majorly in form of a food frequency questionnaire and then percentages and frequencies were calculated for all food groups. In age groups 3-12 years there was a higher consumption of beverages both hot and sweet and nuts and seeds were consumed in higher amounts. On the other hand, the age group 13-18 consumed more fruits and vegetables. Similarly, when moving to age 19-25 and 26-40 there is a higher consumption of milk and milk products. Cereals are consumed most by adults of age 41-60 years and 60+ leaned more towards sweets and snacks. Women tend to consume a more calorie-dense diet than men. Also, children and older adults rely more on sweets and snacks rather than fruits, vegetables, and other nutrient-dense foods.

Rhythmic neuronal activities of the rat nucleus of the solitary tract are impaired by high-fat diet - implications for daily control of satiety.

Temporal partitioning of daily food intake is crucial for survival and involves the integration of internal circadian states and external influences such as the light-dark cycle and dietary composition. These intrinsic and extrinsic factors are interdependent with misalignment of circadian rhythms promoting body weight gain, while consumption of a calorie-dense diet elevates the risk of obesity and blunts circadian rhythms. Recently, we defined the circadian properties of the dorsal vagal complex of the brainstem, a structure implicated in the control of food intake and autonomic tone, but whether and how 24h rhythms in this area are influenced by diet remains unresolved. Here we focused on a key structure of this complex, the nucleus of the solitary tract (NTS). We used a combination of immunohistochemical and electrophysiological approaches together with daily monitoring of body weight and food intake to interrogate how the neuronal rhythms of the NTS are affected by a high-fat diet. We report that short-term consumption of a high-fat diet increases food intake during the day and blunts NTS daily rhythms in neuronal discharge. Additionally, we found that a high-fat diet dampens NTS responsiveness to metabolic neuropeptides, and decreases orexin immunoreactive fibres in this structure. These alterations occur without prominent body weight gain, suggesting that a high-fat diet acts initially to reduce activity in the NTS to disinhibit mechanisms that suppress daytime feeding. KEY POINTS: The dorsal vagal complex of the rodent hindbrain possesses intrinsic circadian timekeeping mechanisms In particular, the nucleus of the solitary tract (NTS) is a robust circadian oscillator, independent of the master suprachiasmatic clock Here, we reveal that rat NTS neurons display timed daily rhythms in their neuronal activity and responsiveness to ingestive cues These daily rhythms are blunted or eliminated by a short-term high-fat diet, together with increased consumption of calories during the behaviourally quiescent day Our results help us better understand the circadian control of satiety by the brainstem and its malfunctioning under a high-fat diet.

Cafeteria Diet Impacts the Body Weight and Energy Expenditure of Brown Norway Rats in an Apparent Age Dependent Manner, but Has no Effect on Muscle Anabolic Sensitivity to Nutrition.

While obesity blunts the ability of muscle to mount a protein synthetic response to an amino acid infusion in older adults, it is unclear if this insensitivity to nutrition persists long term and in response to complete foods is unknown. To address this, young (2 months old) and old (17–20 months old) Brown Norway rats were randomized to receive either chow or a 12 wk diet of calorie-dense human foods. At wk 10 drinking water was supplemented with 2% heavy water, followed 2 weeks later by a flooding dose of [2H5]-phenylalanine and an oral leucine bolus, allowing the short and long-term effects of age and diet on muscle protein synthesis rates to be determined. The experimental diet increased energy intake in both young (7.4 ± 0.9%) and old (18.2 ± 1.8%) animals (P < 0.01), but only led to significant increases in body weight in the former (young: 10.2 ± 3.0% (P < 0.05) and old: 3.1 ± 5.1% (NS) vs. age-matched controls). Notably, energy expenditure in response to the cafeteria diet was increased in old animals only (chow: 5.1 ± 0.4; cafe: 8.2 ± 1.6 kcal.kg b.w−1.h−1; P < 0.05). Gastrocnemius protein fractional synthetic rates in response to either an acute leucine bolus or two weeks of feeding were equivalent across groups irrespective of age or diet. Rodents in old age appear capable of preventing weight gain in response to a calorie-dense diet by increasing energy expenditure while maintaining the anabolic sensitivity of muscle to nutrition; the mechanisms of which could have important implications for the aging obese human.

Modulatory Effect of Intermittent Fasting on Adipose Tissue Inflammation: Amelioration of Cardiovascular Dysfunction in Early Metabolic Impairment.

Cardiometabolic syndrome (CMS) is a cluster of maladaptive cardiovascular, renal, thrombotic, inflammatory, and metabolic disorders. It confers a high risk of cardiovascular mortality and morbidity. CMS is triggered by major shifts in lifestyle and dietary habits with increased consumption of refined, calorie-dense diets. Evidence indicates that diet-induced CMS is linked to Adipose tissue (AT) inflammation. This led to the proposal that adipose inflammation may be involved in metabolic derangements, such as insulin resistance and poor glycemic control, as well as the contribution to the inflammatory process predisposing patients to increased cardiovascular risk. Therefore, in the absence of direct pharmacological interventions for the subclinical phase of CMS, time restricted feeding regimens were anticipated to alleviate early metabolic damage and subsequent comorbidities. These regimens, referred to as intermittent fasting (IF), showed a strong positive impact on the metabolic state of obese and non-obese human subjects and animal models, positive AT remodeling in face of overnutrition and high fat diet (HFD) consumption, and improved CV outcomes. Here, we summarize the available evidence on the role of adipose inflammation in triggering cardiovascular impairment in the context of diet induced CMS with an emphasis on the involvement of perivascular adipose tissue. As well, we propose some possible molecular pathways linking intermittent fasting to the ameliorative effect on adipose inflammation and cardiovascular dysfunction under such circumstances. We highlight a number of targets, whose function changes in perivascular adipose tissue inflammation and could be modified by intermittent fasting acting as a novel approach to ameliorate the inflammatory status.

Atrial Fibrillation and Obesity: Reverse Remodeling of Atrial Substrate With Weight Reduction.

This study sought to evaluate the effect of weight loss on the atrial substrate for atrial fibrillation (AF). Whether weight loss can reverse the atrial substrate of obesity is not known. Thirty sheep had sustained obesity induced by ad libitum calorie-dense diet over 72weeks. Animals were randomized to 3 groups: sustained obesity and 15% and 30% weight loss. The animals randomized to weight loss underwent weight reduction by reducing the quantity of hay over 32weeks. Eight lean animals served as controls. All were subjected to the following: dual-energy x-ray absorptiometry, echocardiogram, cardiac magnetic resonance, electrophysiological study, and histological and molecular analyses (fatty infiltration, fibrosis, transforming growth factor β1, and connexin 43). Sustained obesity was associated with increased left atrium (LA) pressure (p<0.001), inflammation (p<0.001), atrial transforming growth factor β1 protein (p<0.001), endothelin-B receptor expression (p=0.04), atrial fibrosis (p=0.01), epicardial fat infiltration (p<0.001), electrophysiological abnormalities, and AF burden (p=0.04). Connexin 43 expression was decreased in the obese group (p=0.03). In this obese ovine model, 30% weight reduction was associated with reduction in total body fat (p<0.001), LA pressure (p=0.007), inflammation (p<0.001), endothelin-B receptor expression (p=0.01), atrial fibrosis (p=0.01), increase in atrial effective refractory period (cycle length: 400 and 300ms; p<0.001), improved conduction velocity (cycle length: 400 and 300ms; p=0.01), decreased conduction heterogeneity (p<0.001), and decreased AF inducibility (p=0.03). Weight loss was associated with a nonsignificant reduction in epicardial fat infiltration in posterior LA (p=0.34). Weight loss in an obese ovine model is associated with structural and electrophysiological reverse remodeling and a reduced propensity for AF. This provides evidence for the direct role of obesity in AF substrate and the role of weight reduction in patients with AF.

Obesity and endocrine-disrupting chemicals.

Obesity is now a worldwide pandemic. The usual explanation given for the prevalence of obesity is that it results from consumption of a calorie dense diet coupled with physical inactivity. However, this model inadequately explains rising obesity in adults and in children over the past few decades, indicating that other factors must be important contributors. An endocrine-disrupting chemical (EDC) is an exogenous chemical, or mixture that interferes with any aspect of hormone action. EDCs have become pervasive in our environment, allowing humans to be exposed daily through ingestion, inhalation, and direct dermal contact. Exposure to EDCs has been causally linked with obesity in model organisms and associated with obesity occurrence in humans. Obesogens promote adipogenesis and obesity, in vivo, by a variety of mechanisms. The environmental obesogen model holds that exposure to obesogens elicits a predisposition to obesity and that such exposures may be an important yet overlooked factor in the obesity pandemic. Effects produced by EDCs and obesogen exposure may be passed to subsequent, unexposed generations. This “generational toxicology” is not currently factored into risk assessment by regulators but may be another important factor in the obesity pandemic as well as in the worldwide increases in the incidence of noncommunicable diseases that plague populations everywhere. This review addresses the current evidence on how obesogens affect body mass, discusses long-known chemicals that have been more recently identified as obesogens, and how the accumulated knowledge can help identify EDCs hazards.

Exploring the Diets of Adults with Obesity and Type II Diabetes from Nine Diverse Countries: Dietary Intakes, Patterns, and Quality.

Background: Calorie-dense diet is a main driver of the global epidemics of obesity and type 2 diabetes (T2DM). While various dietary strategies and patterns are efficacious in reducing risk and improving glycemic control, dietary intake and diet quality have been inadequately studied among individuals who remain living in their native environments. There is also little published on dietary patterns of diverse ethnic, cultural, or regional populations. Objective: To explore dietary intakes, patterns and overall diet quality in adults with obesity and T2DM from diverse countries. We hypothesized that individuals sharing a common clinical phenotype (age, BMI, years since T2DM diagnosis and inadequate glycemic control) would demonstrate comparable high calorie “western” dietary patterns and low diet quality despite differences in geographic regions and cultures. Design: Diet data were acquired from 611 adults in Argentina, Germany, Poland, Serbia, Slovakia, Slovenia, Spain, Turkey and the USA via three 24-h diet recalls. Contribution of 168 foods to 14 primary food groups was confirmed by Spearman’s rank-order correlations and Principle Component Factor Analysis identified dietary patterns. Diet quality was assessed using the Healthy Eating Index 2015. Results: Eleven dietary patterns were extracted; the most common were a “Mediterranean-like” pattern shared by six countries and a “Calorie Dense” pattern shared by five countries. Also common were “Lacto-Vegetarian, “Pesco-Vegetarian,” and “Vegan” patterns. Only 2.1% of subjects had good diet quality (HEI-2015 score >80). Conclusions: The diet pattern data suggest that influences of more traditional region-specific diets remain. However, overall diet quality was poor and may contribute to inadequate glycemic control, possibly due to excess intake of high calorie/nutrient poor foods, which may be associated with global transitions occurring in the available food supply.

Strain specific variation underlines the disparity in stress response of rats to calorie dense diets in the pathophysiology of obesity

Obesity is a multifactorial disorder, caused mainly due to lifestyle changes, and increased consumption of calorie dense diets is not just limited to developed countries anymore. Chronic physiological stress and oxidative stress are known to be implicated in the etiology of obesity. However, the role of stress response towards obesity manifestation in genetically different rat strains is poorly understood. In the current study we have used obesity susceptible & resistant rat models to understand the role of both glucocorticoid and oxidativestress in the pathophysiology of obesity. Upon challenge with calorie dense diets, WNIN showed an increased glucocorticoid stress, resulting in increased oxidative stress; whereas such a phenomenon was not noticed in F-344 and SD. However, there was an increase in the circulatory melatonin levels in calorie dense fed groups of both F-344 and SD animals, which might have contributed to reduced oxidative stress. The molecular switch in the activation of melatonin could be possibly attributed to the genetic differences among these strains. It will be interesting to explore other molecular mechanisms for melatonin regulation, albeit increased corticosterone is implicated in the enhanced production of melatonin.

Germ-Free Swiss Webster Mice on a High-Fat Diet Develop Obesity, Hyperglycemia, and Dyslipidemia.

A calorie-dense diet is a well-established risk factor for obesity and metabolic syndrome (MetS), whereas the role of the intestinal microbiota (IMB) in the development of diet-induced obesity (DIO) is not completely understood. To test the hypothesis that Swiss Webster (Tac:SW) mice can develop characteristics of DIO and MetS in the absence of the IMB, we fed conventional (CV) and germ-free (GF) male Tac:SW mice either a low-fat diet (LFD; 10% fat derived calories) or a high-fat diet (HFD; 60% fat derived calories) for 10 weeks. The HFD increased feed conversion and body weight in GF mice independent of the increase associated with the microbiota in CV mice. In contrast to CV mice, GF mice did not decrease feed intake on the HFD and possessed heavier fat pads. The HFD caused hyperglycemia, hyperinsulinemia, and impaired glucose absorption in GF mice independent of the increase associated with the microbiota in CV mice. A HFD also elevated plasma LDL-cholesterol and increased hepatic triacylglycerol, free fatty acids, and ceramides in all mice, whereas hypertriglyceridemia and increased hepatic medium and long-chain acylcarnitines were only observed in CV mice. Therefore, GF male Tac:SW mice developed several detrimental effects of obesity and MetS from a high-fat, calorie dense diet.

P6294NLRP3 inflammasome is activated in the atrium of an ovine model of sustained obesity

Abstract Introduction Obesity and enhanced inflammatory response are two independent risk factors involved in the pathogenesis of atrial fibrillation (AF). Components of the NLRP3 inflammasome have been found to be expressed in cardiomyocytes and cardiac fibroblasts and that increased inflammasome activation contributes to the pathogenesis of AF. The NLRP3 inflammasome is a multi-protein signaling complex that is activated in two steps: 1st) a priming event that includes a NFκB-activating stimuli which increases the expression of pro-inflammatory cytokines, and 2nd) a triggering event that includes the assembly of the inflammasome complex and activation of caspase-1 which promotes the production of pro-inflammatory cytokines like interleukin 1 beta (IL-1b). Purpose We used a sheep model of sustained obesity to characterize the association between atrial myocardial fat infiltration, atrial activation of the NLRP3 inflammasome and the development of an atrial arrhythmogenic substrate for AF. Methods Eight sheep were fed ad libitum calorie-dense diet over 40 weeks to gain weight and were maintained in this state of sustained obesity for another 40 weeks. Eight lean, weight-controlled and aged-matched sheep served as control. Atrial fat infiltration was determined by oil-red staining and NLRP3 inflammasome activation was assessed by immunoblot in atrial whole-tissue lysate. Atrial effective refractory periods (aERPs) were evaluated (twice diastolic threshold, cycle length (CL) of 400 ms, S1S2 -protocol). Results Sustained obesity was associated with increased atrial fat infiltration (lean: 0.8±0.3% vs. obese: 2.3±1.2%, p=0.1) and shorter aERP (lean: 169±22ms vs. obese: 138±26ms, p=0.03). Protein levels of caspase-1 and mature IL-1β were significantly enhanced (p=0.04 and p=0.01, respectively). Further shortening of aERP correlated with increasing atrial protein levels of caspase-1 (r=0.59, p=0.02). In contrast, levels of TNFα and NFκB were not significantly changed in atria of sheep with sustained obesity. Conclusions Sustained obesity is associated with increased expression of NLRP3 inflammasome-related proteins and the development of an arrhythmogenic substrate for AF. Our study suggest that the increased activity is due to increased triggering, rather than increased gene transcription. Whether NLRP3 inflammasome activation represents a modifiable target to prevent AF in obesity warrants further study.

In urban, but not rural, areas of Madre de Dios, Peru, adoption of a Western diet is inversely associated with selenium intake

Road development has been a major driver of the transition from traditional to calorie-dense processed ‘Western’ diets in lower and middle-income countries. The paving of the Interoceanic Highway (IOH) facilitated rapid development to the Madre de Dios (MDD) region in the Peruvian Amazon. As traditional foods such as Brazil nuts and fish are known to be rich in the essential micronutrient selenium, people further along the nutrition transition to a Western diet may have lower selenium (Se) intake. To test this hypothesis, in 2014 the Investigacion de Migracion, Ambiente, y Salud (IMAS Study) (Migration, Environment, and Health Study) collected household surveys from 310 households in 46 communities along the IOH and nails for Se analysis from 418 adults. Principal component analysis of 25 commonly consumed food items identified a factor resembling Western diet, which was used to calculate household Western diet weighted sum factor scores (WSFS). WSFS means were interpolated into a 10 km buffer around the IOH using inverse distance weighting. Western diet adoption was higher in urban compared to rural areas (p < 0.0001), and geographic variation was observed between mining and agricultural areas. Mean nail Se was 730 ng/g, SD 198 ng/g (range: 200–1390 ng/g). Generalized estimating equation (GEE) models assessed the association between food consumption and nail Se. Household chicken consumption was positively associated with Se in rural areas only. Urban/rural status modified the effect of western diet adoption on nail Se, and Se was inversely associated with WSFS in urban areas only. Conclusion: In urban, but not rural, areas of Madre de Dios, Peru, adoption of a Western diet is inversely associated with selenium intake. As the essential micronutrient selenium is a vital part of antioxidant proteins, lower intake could compound the chronic health effects that may result from transition to a calorie-dense diet.

Chronic calorie-dense diet drives differences in motivated food seeking between obesity-prone and resistant mice.

Obesity results from overconsumption of energy, partly because of the inability to refrain from highly palatable rewarding foods. Even though palatable food is available to everyone, only a fraction of the population develops obesity. We previously showed that following chronic exposure to highly palatable food animals that gained the most weight also showed addictive-like motivation to seek for palatable food. An important question remains-is this extreme, addictive-like, motivation to consume palatable food the cause or the consequence of diet-induced obesity? Here, we show that obesity-prone (OP) mice exhibit higher motivation for palatable food consumption compared with obesity-resistant mice even before developing obesity, but that the full manifestation of this high motivation to eat is expressed only after chronic exposure to high-fat-high-sugar (HFHS) diet. HFHS diet also impairs performance in the operant food-seeking task selectively in OP mice, an impairment that persists even after 2weeks of abstinence from HFHS food. Overall, our data suggest that while some aspects of food motivation are high in OP mice already before developing obesity, the chronic exposure to HFHS food accentuates it and drives the development of obesity.

Effect of nitroso-redox imbalance on male reproduction.

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are byproducts of normal metabolic processes. They are necessary for normal cellular function and are kept in balance by antioxidant mechanisms. Alterations in levels of ROS and RNS can lead to nitroso-redox imbalance that in turn can negatively affect male reproduction. Strategies to decrease ROS/RNS involve evasion of exposures (smoking, meat intake, pollution, calorie-dense diet), managing lifestyle, and increasing the consumption of antioxidants (vitamin C, vitamin E, alpha-lipoic acid, taurine, quercetin). Targeted therapies focusing on nitroso-redox imbalance can be critical for treatment of male reproductive dysfunction. This review outlines endogenous and exogenous sources of ROS/RNS, adverse effect on male reproduction, and strategies to control nitroso-redox imbalance.

Intravenous administration of oxytocin in rats acutely decreases deprivation-induced chow intake, but it fails to affect consumption of palatable solutions

Despite its limited ability to cross the blood-brain barrier, peripherally administered oxytocin (OT) acutely decreases food intake, most likely via the brainstem and hypothalamic mechanisms. Studies performed to date have focused mainly on the effects of subcutaneous or intraperitoneal OT on the consumption of only solid calorie-dense diets (either standard or high-fat), whereas it is unknown whether, similarly to central OT, peripherally administered peptide reduces intake of calorie-dilute and non-caloric palatable solutions. In this project, we established that 0.1μg/kg intravenous (IV) OT is the lowest anorexigenic dose, decreasing deprivation-induced standard chow intake by ca. 40% in rats and its effect does not stem from aversion. We then used this dose in paradigms in which effects of centrally acting OT ligands on consumption of palatable solutions had been previously reported. We found that IV OT did not change episodic intake of individually presented palatable solutions containing 10% sucrose, 0.1% saccharin, combined 10% sucrose-0.1% saccharin or 4.1%. Intralipid and it failed to affect daily scheduled consumption of a sucrose solution in non-deprived rats. In a two-bottle choice test, IV OT did not shift animals’ preference from sucrose to Intralipid. Finally, OT injected IV prior to the simultaneous presentation chow and a sucrose solution in food-deprived rats significantly decreased chow intake, whereas sugar water consumption remained unchanged. We conclude that IV OT reduces deprivation-induced chow intake without causing aversion, but the dose effective in decreasing energy-driven consumption of high-calorie food fails to affect consumption of palatable calorie-dilute solutions.

Electrophysiological, Electroanatomical, and Structural Remodeling of the Atria as Consequences of Sustained Obesity

BackgroundObesity and atrial fibrillation (AF) are public health issues with significant consequences. ObjectivesThis study sought to delineate the development of global electrophysiological and structural substrate for AF in sustained obesity. MethodsTen sheep fed ad libitum calorie-dense diet to induce obesity over 36 weeks were maintained in this state for another 36 weeks; 10 lean sheep with carefully controlled weight served as controls. All sheep underwent electrophysiological and electroanatomic mapping; hemodynamic and imaging assessment (echocardiography and dual-energy x-ray absorptiometry); and histology and molecular evaluation. Evaluation included atrial voltage, conduction velocity (CV), and refractoriness (7 sites, 2 cycle lengths), vulnerability for AF, fatty infiltration, atrial fibrosis, and atrial transforming growth factor (TGF)-β1 expression. ResultsCompared with age-matched controls, chronically obese sheep demonstrated greater total body fat (p < 0.001); LA volume (p < 0.001); LA pressure (p < 0.001), and PA pressures (p < 0.001); reduced atrial CV (LA p < 0.001) with increased conduction heterogeneity (p < 0.001); increased fractionated electrograms (p < 0.001); decreased posterior LA voltage (p < 0.001) and increased voltage heterogeneity (p < 0.001); no change in the effective refractory period (ERP) (p > 0.8) or ERP heterogeneity (p > 0.3). Obesity was associated with more episodes (p = 0.02), prolongation (p = 0.01), and greater cumulative duration (p = 0.02) of AF. Epicardial fat infiltrated the posterior LA in the obese group (p < 0.001), consistent with reduced endocardial voltage in this region. Atrial fibrosis (p = 0.03) and TGF-β1 protein (p = 0.002) were increased in the obese group. ConclusionsSustained obesity results in global biatrial endocardial remodeling characterized by LA enlargement, conduction abnormalities, fractionated electrograms, increased profibrotic TGF-β1 expression, interstitial atrial fibrosis, and increased propensity for AF. Obesity was associated with reduced posterior LA endocardial voltage and infiltration of contiguous posterior LA muscle by epicardial fat, representing a unique substrate for AF.